Publications by authors named "Guangquan Xu"

12 Publications

  • Page 1 of 1

Formation environments and mechanisms of multistage paleokarst of Ordovician carbonates in Southern North China Basin.

Sci Rep 2021 Jan 12;11(1):819. Epub 2021 Jan 12.

Department of Geology and Hydrogeology, Huaihe Energy Holding Group Co., Ltd., Huainan, 232001, China.

With the reduction of oil and gas reserves and the increase of mining difficulty in Northern China, the carbonate rocks in Southern North China Basin are becoming a significant exploration target for carbonate reservoirs. However, the development characteristics, formation stages, formation environments and mechanisms of the carbonate reservoirs in Southern North China Basin are still unclear, which caused the failures of many oil and gas exploration wells. This study focused on addressing this unsolved issue from the Ordovician carbonate paleokarst in the Huai-Fu Basin, which is located in the southeast of Southern North China Basin and one of the key areas for oil and gas exploration. Based on petrology, mineralogy and geochemical data, pore types, distribution characteristics, and formation stages of the Ordovician paleokarst were analyzed. Then, in attempt to define the origins of porosity development, the formation environments and mechanisms were illustrated. The results of this study showed that pore types of the Ordovician carbonates in the Huai-Fu Basin are mainly composed of intragranular pores, intercrystalline (intergranular) pores, dissolution pores (vugs), fractures, channels, and caves, which are usually in fault and fold zones and paleoweathering crust. Furthermore, five stages and five formation environments of the Ordovician paleokarst were identified. Syngenetic karst, eogenetic karst, and paleoweathering crust karst were all developed in a relatively open near-surface environment, and their formations are mainly related to meteoric water dissolution. Mesogenetic karst was developed in a closed buried environment, and its formation is mainly related to the diagenesis of organic matters and thermochemical sulfate reduction in the Permian-Carboniferous strata. Hydrothermal (water) karst was developed in a deep-buried and high-temperature environment, where hydrothermal fluids (waters) migrated upward through structures such as faults and fractures to dissolve carbonate rocks and simultaneously deposited hydrothermal minerals and calcites. Lastly, a paleokarst evolution model, combined with the related porosity evolution processes, nicely revealed the Ordovician carbonate reservoir development. This study provides insights and guidance for further oil and gas exploration in the Southern North China Basin, and also advances our understanding of the genesis of carbonate paleokarst around the world.
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http://dx.doi.org/10.1038/s41598-020-80878-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7804134PMC
January 2021

The effects of β-TCP on mechanical properties, corrosion behavior and biocompatibility of β-TCP/Zn-Mg composites.

Mater Sci Eng C Mater Biol Appl 2020 Mar 5;108:110397. Epub 2019 Nov 5.

Tianjin Key Laboratory for Photoelectric Materials and Devices, Tianjin 300384, China. Electronic address:

Zinc has attracted increasing attention in the field of degradable implant materials due to its suitable degradation rate. To further improve the mechanical properties and biocompatibility of zinc, Zn-1Mg-nvol%β-TCP (n = 0, 1, 3, 5) composites were fabricated for biomedical application by the mechanical stirring combined with ultrasonic assisted casting and hot extrusion technology. The microstructure, mechanical properties and corrosion behavior of these composites were systemically investigated and the composite with the best comprehensive performance were selected for biocompatibility evaluation including L-929 cells cytotoxicity test and SD rat model experiment. Tensile test revealed that Zn-1Mg-1vol%β-TCP composite possessed optimal mechanical properties. The yield strength (YS), ultimate tensile strength (UTS), elongation (σ) and elastic modulus (E) of the as-extruded Zn-1Mg-1vol%β-TCP composite are 250.8 MPa, 330.5 MPa, 11.7% and 125.4 GPa respectively. The immersion tests showed that the corrosion resistance of the composite is slightly decreased with the increase of β-TCP content. In addition, the addition of β-TCP makes the cytocompatibility of the composites better than that of the Zn-1Mg alloy matrix. Various blood biochemical parameters in rat serum samples after implantation showed Zn-1Mg alloy and Zn-1Mg-β-TCP composites has not significant tissue inflammation and showed good biocompatibility.
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http://dx.doi.org/10.1016/j.msec.2019.110397DOI Listing
March 2020

Transcription Factor p53 Suppresses Tumor Growth by Prompting Pyroptosis in Non-Small-Cell Lung Cancer.

Oxid Med Cell Longev 2019 13;2019:8746895. Epub 2019 Oct 13.

Department of Thoracic Surgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150081, China.

Objective: To evaluate the effect of p53 on pyroptosis and its inhibitory role on tumor growth in non-small-cell lung cancer (NSCLC).

Methods: The correlation of p53 and pyroptosis was determined in tumor tissues of NSCLC patients. The pyroptotic level was detected in A549 cells to clarify the effect of p53 on pyroptosis. p53 overexpression A549 tumor-bearing mice were used to clarify the therapeutic target of p53 in NSCLC treatment.

Results: p53 expression level was positively related to pyroptosis in NSCLC tissues. In assays, p53 directly regulated pyroptosis in A549 cells. p53-specific knockdown blocked lipopolysaccharide- (LPS-) induced pyroptosis. In assays, p53 overexpression in A549 markedly decreased tumor growth and death rate by increasing the pyroptotic level.

Conclusions: Upregulation of p53 prompts pyroptosis to produce anti-NSCLC effects suggesting the potential of p53 on suppressing tumor growth in NSCLC patients.
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http://dx.doi.org/10.1155/2019/8746895DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6815571PMC
May 2020

Generalized Centered 2-D Principal Component Analysis.

IEEE Trans Cybern 2021 Mar 17;51(3):1666-1677. Epub 2021 Feb 17.

Most existing robust principal component analysis (PCA) and 2-D PCA (2DPCA) methods involving the l -norm can mitigate the sensitivity to outliers in the domains of image analysis and pattern recognition. However, existing approaches neither preserve the structural information of data in the optimization objective nor have the robustness of generalized performance. To address the above problems, we propose two novel center-weight-based models, namely, centered PCA (C-PCA) and generalized centered 2DPCA with l -norm minimization (GC-2DPCA), which are developed for vector- and matrix-based data, respectively. The C-PCA can preserve the structural information of data by measuring the similarity between the data points and can also retain the PCA's original desirable properties such as the rotational invariance. Furthermore, GC-2DPCA can learn efficient and robust projection matrices to suppress outliers by utilizing the variations between each row of the image matrix and employing power p of l -norm. We also propose an efficient algorithm to solve the C-PCA model and an iterative optimization algorithm to solve the GC-2DPCA model, and we theoretically analyze their convergence properties. Experiments on three public databases show that our models yield significant improvements over the state-of-the-art PCA and 2DPCA approaches.
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http://dx.doi.org/10.1109/TCYB.2019.2931957DOI Listing
March 2021

Fabrication of biodegradable HA/Mg-Zn-Ca composites and the impact of heterogeneous microstructure on mechanical properties, in vitro degradation and cytocompatibility.

Bioelectrochemistry 2019 Oct 6;129:106-115. Epub 2019 May 6.

School of Mechanical, Materials & Mechatronic Engineering, University of Wollongong, NSW 2522, Australia; ARC Research Hub for Australian Steel Manufacturing, University of Wollongong, NSW, Australia.

Due to their desirable elastic modulus and density that are similar to natural bone, non-toxic element containing magnesium alloys are regarded as promising bio-degradable materials. A biodegradable HA-particle-reinforced magnesium-matrix composite Mg-3Zn-0.2Ca-1HA (wt%) was fabricated for biomedical application by a combination of high shear solidification (HSS) and hot extrusion technology. The microstructure, mechanical properties, corrosion resistance and cell biocompatibility of the composite were subsequently investigated. In comparison with the matrix alloy, the as-cast Mg-3Zn-0.2Ca-1HA composite obtained by HSS technology exhibited a uniform and fine grained structure, further refined after a hot extrusion ratio of 36:1. The yield strength (0.2%YS), ultimate tensile strength and elongation of the extruded composite were 322 MPa, 341 MPa and 7.6%, respectively. The corrosion rate of the as-extruded Mg-3Zn-0.2Ca-1HA composite was measured to be 1.52 mm/y. Electrochemical and immersion tests showed that the corrosion resistance of the composite is slightly improved comparing to that of the matrix alloy.
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http://dx.doi.org/10.1016/j.bioelechem.2019.05.001DOI Listing
October 2019

Circular RNA hsa_circ_0008305 (circPTK2) inhibits TGF-β-induced epithelial-mesenchymal transition and metastasis by controlling TIF1γ in non-small cell lung cancer.

Mol Cancer 2018 09 27;17(1):140. Epub 2018 Sep 27.

Soochow University Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, 199 Ren'ai Road, Suzhou, 215123, Jiangsu, China.

Background: TGF-β promotes tumor invasion and metastasis through inducing epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC). Circular RNAs (circRNAs) are recognized as functional non-coding RNAs involved in human cancers. However, whether and how circRNAs contribute to TGF-β-induced EMT and metastasis in NSCLC remain vague. Here, we investigated the regulation and function of Circular RNA hsa_circ_0008305 (circPTK2) in TGF-β-induced EMT and tumor metastasis, as well as a link between circPTK2 and transcriptional intermediary factor 1 γ (TIF1γ) in NSCLC.

Methods: Circular RNAs were determined by human circRNA Array analysis, real-time quantitative reverse transcriptase PCR and northern blot. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP), RNA pull-down and fluorescence in situ hybridization (FISH) assays were employed to test the interaction between circPTK2 and miR-429/miR-200b-3p. Ectopic overexpression and siRNA-mediated knockdown of circPTK2, TGF-β-induced EMT, Transwell migration and invasion in vitro, and in vivo experiment of metastasis were used to evaluate the function of circPTK2. Transcription and prognosis analyses were done in public databases.

Results: CircPTK2 and TIF1γ were significantly down-regulated in NSCLC cells undergoing EMT induced by TGF-β. CircPTK2 overexpression augmented TIF1γ expression, inhibited TGF-β-induced EMT and NSCLC cell invasion, whereas circPTK2 knockdown had the opposite effects. CircPTK2 functions as a sponge of miR-429/miR-200b-3p, and miR-429/miR-200b-3p promote TGF-β-induced EMT and NSCLC cell invasion by targeting TIF1γ. CircPTK2 overexpression inhibited the invasion-promoting phenotype of endogenous miR-429/miR-200b-3p in NSCLC cells in response to TGF-β. CircPTK2 overexpression significantly decreased the expression of Snail, an important downstream transcriptional activator of TGF-β/Smad signaling. In an in vivo experiment of metastasis, circPTK2 overexpression suppressed NSCLC cell metastasis. Moreover, circPTK2 expression was dramatically down-regulated and positively correlated with TIF1γ expression in human NSCLC tissues. Especially, circPTK2 was significantly lower in metastatic NSCLC tissues than non-metastatic counterparts.

Conclusion: Our findings show that circPTK2 (hsa_circ_0008305) inhibits TGF-β-induced EMT and metastasis by controlling TIF1γ in NSCLC, revealing a novel mechanism by which circRNA regulates TGF-β-induced EMT and tumor metastasis, and suggesting that circPTK2 overexpression could provide a therapeutic strategy for advanced NSCLC.
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http://dx.doi.org/10.1186/s12943-018-0889-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6161470PMC
September 2018

Long non-coding RNA XIST promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-367/141-ZEB2 axis in non-small-cell lung cancer.

Cancer Lett 2018 04 17;418:185-195. Epub 2018 Jan 17.

Soochow University Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, Jiangsu, 215123, China; Department of Genetics, School of Biology and Basic Medical Science, Medical College of Soochow University, Suzhou, Jiangsu, 215123, China; Suzhou Key Laboratory for Molecular Cancer Genetics, Suzhou, Jiangsu, 215123, China. Electronic address:

Growing evidence shows that lncRNA XIST functions as an oncogene accelerating tumor progression. Transforming growth factor β (TGF-β)-induced epithelial-mesenchymal transition (EMT) plays a key role in tumor metastasis. However, it is still unclear whether lncRNA XIST is implicated in TGF-β-induced EMT and influences cell invasion and metastasis in non-small-cell lung cancer (NSCLC). Here, we observed increased expression of lncRNA XIST and ZEB2 mRNA in metastatic NSCLC tissues. Knockdown of lncRNA XIST inhibited ZEB2 expression, and repressed TGF-β-induced EMT and NSCLC cell migration and invasion. Being in consistent with the in vitro findings, the in vivo experiment of metastasis showed that knockdown of lncRNA XIST inhibited pulmonary metastasis of NSCLC cells in mice. In addition, knockdown of ZEB2 expression can inhibit TGF-β-induced EMT and NSCLC cell migration and invasion. Mechanistically, lncRNA XIST and ZEB2 were targets of miR-367 and miR-141. Furthermore, both miR-367 and miR-141 expression can be upregulated by knockdown of lncRNA XIST. Taken together, our study reveals that lncRNA XIST can promote TGF-β-induced EMT and cell invasion and metastasis by regulating miR-367/miR-141-ZEB2 axis in NSCLC.
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http://dx.doi.org/10.1016/j.canlet.2018.01.036DOI Listing
April 2018

Cordycepin inhibits LPS-induced acute lung injury by inhibiting inflammation and oxidative stress.

Eur J Pharmacol 2018 Jan 18;818:110-114. Epub 2017 Oct 18.

Department of Thoracic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150081, China. Electronic address:

Acute lung injury (ALI) is a common severe clinical syndrome in intensive care unit. Inflammation has been reported to play a critical role in the development of ALI. Cordycepin, an active component isolated from Cordyceps militaris, has been reported to have anti-inflammatory effects. However, the anti-inflammatory effects of cordycepin on LPS-induced ALI remain unclear. Therefore, in the present study, we assessed whether cordycepin could attenuate ALI induced by LPS. The mice were conditioned with cordycepin 1h before intranasal instillation of LPS. Lung wet/dry (W/D) ratio, MPO activity, MDA content, and inflammatory cytokines production were detected. The expression of NF-κB p65, I-κB, Nrf2, and HO-1 were detected by western blot analysis. We found that LPS significantly increased lung wet/dry (W/D) ratio, MPO activity, MDA content, and inflammatory cytokines production. However, the increases were significantly inhibited by treatment of cordycepin. LPS-induced NF-κB activation was also suppressed by cordycepin. In addition, cordycepin was found to up-regulate the expression of Nrf2 and HO-1 in a dose-dependent manner. In conclusion, our results demonstrated that cordycepin could attenuate LPS-induced ALI effectively, probably due to inhibition of inflammation and oxidative stress.
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http://dx.doi.org/10.1016/j.ejphar.2017.10.029DOI Listing
January 2018

Artesunate Protects LPS-Induced Acute Lung Injury by Inhibiting TLR4 Expression and Inducing Nrf2 Activation.

Inflammation 2017 Jun;40(3):798-805

Department of Thoracic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.

Artesunate, a derivative of artemisinin, has been reported to have anti-inflammatory property. However, few studies showed the protective effects of artesunate on lung injury. In this study, we aimed to investigate the effects of artesunate on LPS-induced lung injury in mice. The mice were treated with artesunate 1 h before or after LPS treatment. The effects of artesunate on lung MPO activity and malondialdehyde (MDA) content were detected. The lung wet/dry radio and the numbers of inflammatory cells in BALF were also measured. ELISA was used to evaluate the levels of TNF-α, IL-1β, and IL-6 in BALF. Western blot analysis was adapted to detect TLR4 and Nrf2 signaling pathways. The results showed that artesunate protected against LPS-induced ALI by decreasing the numbers of inflammatory cells, lung edema, MPO activity, and MDA content. Furthermore, artesunate significantly inhibited the levels of TNF-α, IL-1β, and IL-6. Artesunate also inhibited LPS-induced IL-6 and IL-8 production in the A549 cells. In addition, artesunate dose-dependently suppressed LPS-induced TLR4 expression and NF-κB activation. The expression of Nrf2 and HO-1 were also up-regulated by artesunate. The data suggest that artesunate possesses anti-inflammatory and anti-oxidant properties against LPS-induced ALI via inhibiting TLR4 signaling pathway and activating Nrf2 signaling pathway.
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http://dx.doi.org/10.1007/s10753-017-0524-6DOI Listing
June 2017

Acanthoic acid ameliorates lipopolysaccharide-induced acute lung injury.

Eur J Pharmacol 2015 Mar 23;750:32-8. Epub 2015 Jan 23.

Department of Thoracic Surgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China. Electronic address:

Acanthoic acid, a pimaradiene diterpene isolated from Acanthopanax koreanum, has been reported to have anti-inflammatory activities. However, the effects of acanthoic acid on LPS-induced acute lung injury have not been reported. The purpose of this study was to investigate the protective effect of acanthoic acid on LPS-induced ALI and to clarify the possible anti-inflammatory mechanisms. In vivo, an LPS-induced ALI model in mice was used to assess the protective effects of acanthoic acid on ALI. Meanwhile, mouse alveolar macrophages MH-S were stimulated with LPS in the presence or absence of acanthoic acid. The expressions of TNF-α, IL-6 and IL-1β were measured by ELISA. LXRα and NF-κB expression were detected by Western blot analysis. The results showed that acanthoic acid downregulated LPS-induced TNF-α, IL-6 and IL-1β production in BALF. MPO activity and lung wet-to-dry ratio were also inhibited by acanthoic acid. In addition, acanthoic acid attenuated lung histopathologic changes. In vitro, acanthoic acid inhibited inflammatory cytokines TNF-α, IL-6 and IL-1β production and NF-κB activation in LPS-stimulated alveolar macrophages. Acanthoic acid was found to up-regulated the expression of LXRα. The inhibition of acanthoic acid on LPS-induced cytokines and NF-κB activation can be abolished by LXRα siRNA. In conclusion, our results suggested that the protective effect of acanthoic acid on LPS-induced ALI was due to its ability to activate LXRα, thereby inhibiting LPS-induced inflammatory response.
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http://dx.doi.org/10.1016/j.ejphar.2015.01.023DOI Listing
March 2015

Prognostic significance of sphingosine kinase 2 expression in non-small cell lung cancer.

Tumour Biol 2014 Jan 7;35(1):363-8. Epub 2013 Aug 7.

Department of Cardiothoracic Surgery, The Second Affiliated Hospital, Harbin Medical University, Harbin, 150086, China.

Sphingosine kinase 2 (SphK2) as a conserved lipid kinase has not been thoroughly elucidated in non-small cell lung cancer (NSCLC). The aim of the present study was to evaluate the expression of SphK2 in NSCLC tissues and to determine its correlation with clinicopathologic characteristics and its impact on patient prognosis. We assessed the expression of SphK2 and proliferating cell nuclear antigen (PCNA) (as a proliferative index) by immunohistochemistry in 180 NSCLC patient's formalin-fixed paraffin-embedded tissue blocks. Relationship between the expression of SphK2 and PCNA and various clinicopathological features in these patients was evaluated. We detected that expression of SphK2 was gradually upregulated from normal, metaplasia/dysplasia tissues to NSCLC tissues. At the same time, PCNA expression followed a similar pattern. Statistical analysis showed that expression of SphK2 in NSCLC tissues was strongly associated with PCNA expression, histology grade, live vaccine strain invasion, lymph node status, clinical stage, tumors size, and histology type. Patients with SphK2 overexpression in their tissues had lower overall survival (OS) and disease-free survival (DFS) rates than those with low SphK2 expression. Using uni- and multivariate analysis, we found that SphK2 overexpression was an independent prognostic factor for both OS and DFS. The expression of SphK2 parallels the progression of NSCLC, and SphK2 overexpression may represent a novel and potentially independent biomarker for the prognosis of patients with NSCLC.
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http://dx.doi.org/10.1007/s13277-013-1051-1DOI Listing
January 2014

Association between p53 codon 72 genetic polymorphisms and tobacco use and lung cancer risk in a Chinese population.

Mol Biol Rep 2013 Jan 11;40(1):645-9. Epub 2012 Oct 11.

Department of Thoracic Surgery, The 2nd Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin 150086, Heilongjiang, China.

Genetic polymorphisms of p53 codon 72 are thought to have significant effects on the metabolism of environmental carcinogens and thus on lung cancer risk, but the reported results are not always consistent. The aim of this study is to investigate the relationship between p53 codon 72 genetic polymorphisms and tobacco use and lung cancer risk in a Chinese population. A population-based control study was conducted in 360 lung cancer patients and 360 cancer-free controls. The genotype of the p53 codon 72 was determined by using a polymerase chain reaction-restriction fragment length polymorphism assay. Patients with lung cancer had a significantly lower frequency of Pro/Pro genotype [odds ratio (OR) = 0.58, 95 % confidence interval (CI) = 0.40, 0.84; P = 0.004] and Pro allele (OR = 0.72, 95 % CI = 0.59, 0.89; P = 0.002) than controls. Patients with squamous cell carcinoma had also a significantly lower frequency of Pro/Pro genotype (OR = 0.45, 95 % CI = 0.25, 0.82; P = 0.009). In the analysis combining p53 codon 72 polymorphisms and smoking, smokers who had smoked for more than 30 pack-years had a significantly lower frequency of Pro/Pro genotype (OR = 0.52, 95 % CI = 0.30, 0.92; P = 0.03) compared with non-smokers. This study suggests that p53 codon 72 polymorphisms play a role in the development of lung cancer and modifies the risk for smoking-related lung cancer in a Chinese population.
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http://dx.doi.org/10.1007/s11033-012-2103-0DOI Listing
January 2013